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Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell+Host+Microbe 2018 ; 23 (2): 203-214.e5 Nephropedia Template TP
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BACTEROIDES FRAGILIS TOXIN COORDINATES A PRO-CARCINOGENIC INFLAMMATORY CASCADE VIA TARGETING OF COLONIC EPITHELIAL CELLS #MMPMID29398651
Chung L; Orberg ET; Geis AL; Chan JL; Fu K; DeStefano Shields CE; Dejea CM; Fathi P; Chen J; Finard BB; Tam AJ; McAllister FM; Fan H; Wu X; Ganguly S; Lebid A; Metz P; Van Meerbeke SW; Huso DL; Wick EC; Pardoll DM; Wan F; Wu S; Sears CL; Housseau F
Cell Host Microbe 2018[Feb]; 23 (2): 203-214.e5 PMID29398651show ga
Pro-carcinogenic bacteria have the potential to initiate and/or promote colon cancer, in part via immune mechanisms that are incompletely understood. Using ApcMin mice colonized with the human pathobiont enterotoxigenic Bacteroides fragilis (ETBF) as a model of microbial-induced colon tumorigenesis, we show that the Bacteroides fragilis toxin (BFT) triggers a pro-carcinogenic multi-step inflammatory cascade requiring IL-17R, NF-?B, and Stat3 signaling in colonic epithelial cells (CECs). Although necessary, Stat3 activation in CECs is not sufficient to trigger ETBF colon tumorigenesis. Notably, IL-17-dependent NF-?B activation in CECs induces a proximal to distal mucosal gradient of C-X-C chemokines, including CXCL1 that mediates the recruitment of CXCR2-expressing polymorphonuclear immature myeloid cells with parallel onset of ETBF-mediated distal colon tumorigenesis. Thus, BFT induces a procarcinogenic signaling relay from the CEC to a mucosal Th17 response that results in NF?B activation selectively in distal colon CECs, that collectively triggers myeloid cell-dependent distal colon tumorigenesis.